Journal
CELL HOST & MICROBE
Volume 16, Issue 1, Pages 115-127Publisher
CELL PRESS
DOI: 10.1016/j.chom.2014.06.001
Keywords
-
Categories
Funding
- NIH [R37 DK057665, R37 AI048638, U19 AI090023, U19 AI057266, U54 AI057157, N01 AI50019, N01 AI50025]
- Bill & Melinda Gates Foundation
- [PS10D11132]
Ask authors/readers for more resources
Dengue virus (DENV) infection induces the expansion of plasmablasts, which produce antibodies that can neutralize DENV but also enhance disease upon secondary infection with another DENV serotype. To understand how these immune responses are generated, we used a systems biological approach to analyze immune responses to dengue in humans. Transcriptomic analysis of whole blood revealed that genes encoding proinflammatory mediators and type I interferon-related proteins were associated with high DENV levels during initial symptomatic disease. Additionally, CD14(+)CD16(+) monocytes increased in the blood. Similarly, in a nonhuman primate model, DENV infection boosted CD14(+)CD16(+) monocyte numbers in the blood and lymph nodes. Upon DENV infection in vitro, monocytes upregulated CD16 and mediated differentiation of resting B cells to plasmablasts as well as immunoglobulin G (IgG) and IgM secretion. These findings provide a detailed picture of innate responses to dengue and highlight a role for CD14(+)CD16(+) monocytes in promoting plasmablast differentiation and anti-DENV antibody responses.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available